Neutrophils redistribute damage across organs

This proposed hypothesis asks whether helping injured muscle could shift inflammatory damage to the heart or lungs. It proposes suppressing EP2, a receptor for the inflammatory signal prostaglandin E2, while blocking neutrophil engulfment, the removal of inflammation-driving immune cells by macrophages. Neutrophils marked for tracking would leave the original tissue, persist in blood and enter distant organs. Early muscle improvement would coincide with delayed heart or lung decline after repeated routine challenges. Months of improvement across muscle, heart and lungs, with no transfer of neutrophil burden, would refute this mechanism. Testing requires cell tracking at the tissue site and in blood, repeated measurements of all three organs, and long-term follow-up.